Brown K A, Lewis S M, Hill T A, Macey M G, McCarthey D A, Grant V A, Treacher D F
Department of Immunobiology, Guy's Hospital Medical School, London, UK.
Perfusion. 2001 Mar;16 Suppl:75-83. doi: 10.1177/026765910101600i111.
The abnormal interaction of polymorphonuclear cells (PMNs) with blood vessel walls is considered to underlie the multiple organ failure of systemic inflammatory response syndrome (SIRS). This consideration is supported by the present finding that PMNs from patients with SIRS are activated, as assessed by an increased distribution of cells bearing CD64, enhanced expression of CD11b and decreased expression of CD62L, and are highly adhesive to endothelial monolayers. Passage of SIRS blood through leucodepletion filters in a laboratory-designed extracorporeal circuit resulted in a marked depletion of PMNs. Of the PMNs that remained in the blood, far fewer cells bound to cultured endothelial cells in comparison with PMNs prior to leucofiltration. We propose that leucofiltration of SIRS blood will limit the number of PMNs available for binding to blood vessel walls and, hence, reduce the pathological manifestations associated with this disorder.
多形核细胞(PMNs)与血管壁的异常相互作用被认为是全身炎症反应综合征(SIRS)多器官功能衰竭的基础。这一观点得到了目前研究结果的支持,即通过携带CD64的细胞分布增加、CD11b表达增强和CD62L表达降低来评估,SIRS患者的PMNs被激活,并且对内皮单层具有高度粘附性。在实验室设计的体外循环中,SIRS血液通过白细胞滤除器后,PMNs显著减少。与白细胞过滤前的PMNs相比,留在血液中的PMNs与培养的内皮细胞结合的细胞要少得多。我们认为,对SIRS血液进行白细胞过滤将限制可与血管壁结合的PMNs数量,从而减少与该疾病相关的病理表现。